The use of dendritic cells (DCs) to prime responses to tumor-associated antigens (TAAs) provides a promising approach to cancer immunotherapy (Palucka et al., Immunity 33, 464-478 (2010)), but clinically-relevant responses have frequently been disappointing (Engell-Noerregaard et al., Cancer Immunol. Immunother. 58, 1-14 (2009); and Robson et al., Curr. Opin. Immunol. 22, 137-144 (2010)). This is partly due to the properties of the DCs most commonly used. Currently, autologous DC, differentiated in vitro from the patient's own peripheral blood monocytes, remain the preferred source of cells for cancer immunotherapy. These monocyte-derived DCs (MoDCs) show significant donor-to-donor variation, which is frequently compounded by the side-effects of chemotherapy. Furthermore, moDCs display a limited capacity for cross-priming of antigen specific CD8+ cytotoxic T lymphocytes (CTLs), creating a dependence on the use of exogenous peptides derived from TAAs and further restricting the scope of such an approach to those HLA haplotypes for which the immunodominant epitopes are known. Since CD8α+ DC in mice are peculiarly capable of cross-presentation, the recent identification of CD141+XCR1+ DC as their functional equivalent in humans (Bachem et al., J. Exp. Med. 207, 1273-1281 (2010); and Crozat et al., J. Exp. Med. 207, 1283-1292 (2010)) has suggested that this subset may be better suited to the induction of anti-tumor responses (Gallois & Bhardwaj, Nature Med. 16, 854-856 (2010)). However, such cells are only present in trace numbers in peripheral blood and low yields are obtained following the culture of progenitors from cord blood (Poulin et al., J. Exp. Med. 207, 1261-1271 (2010)). As a result, they do not represent a feasible treatment for cancer.